Introduction:

Air pollution is caused by the contamination of indoor or outdoor environments by chemical, physical, or biological agents. The World Health Organization (WHO) reports particulate matter (PM), carbon monoxide (CO), ozone (O₃), nitrogen dioxide (NO₂), and sulphur dioxide (SO₂) as pollutants of major public health concern.(1) Both outdoor or ambient and household air pollution (HAP), also known as indoor air pollution (IAP), pose serious health risks.(2) Statistics suggest that the health impacts of HAP far outweigh those of outdoor air pollution, especially in developing countries. HAP can be up to ten times worse than outdoor air pollution because enclosed spaces allow pollutants to accumulate more than open spaces.(3) HAP is estimated to risk the health of around 2.6 billion people who do not have access to clean cooking fuel and who are still dependent on biomass or solid fuels for cooking.(4) Around 3.8 million premature deaths were attributable to HAP in 2016, among these deaths, 27% were due to pneumonia, 18% from stroke, 27% from ischemic heart disease (IHD), 20% from chronic obstructive pulmonary disease (COPD) and 8% from lung cancer. (5)

The principal sources of HAP are the combustion of fuels or other items; however, incomplete combustion of biomass is the main source of HAP worldwide. (6) Inefficient combustion of solid fuels results in products of incomplete combustion, including particles, gases, and a multitude of compounds that are known toxicants. (7) Exposure to such toxic pollutants and PM increases the risk of developing several diseases that have been majorly categorised into categories such as cardiovascular, neurological, respiratory, and cancer. (8)

PM emitted by common solid fuels, in particular, is of concern due to its ability to cross the alveolar membrane and enter the circulation, where it can interact directly with the vascular endothelium and cardiac cells, ultimately leading to cardiovascular diseases. (9)

High BP or hypertension (HTN) is one of the leading global risk factors for cardiovascular diseases, affecting more than one billion individuals and causing 9.4 million deaths each year. (10) Every 20 mmHg increase in systolic blood pressure (SBP) or 10 mmHg increase in diastolic blood pressure (DBP) above 115/75 mmHg has been shown to be associated with more than a two-fold increase in cardiovascular mortality. (11) Because PM2.5 and high BP are both independently leading risk factors for premature death around the world, several researchers have investigated the potential link between these two factors.

In 2008, Fullerton and colleagues published a non-systematic review of research on the health effects of HAP from biomass fuel, including cardiovascular disease, and found a scarcity of relevant data. (12) In another review article published in 2016, only a section of the paper discusses the relationship between IAP exposure and BP. (13) A systematic review by Zafar and David assessed the strength of the evidence for an association of coronary heart disease with HAP from solid fuel use and the likely magnitude of any increase in risk. (14) However, over the last few years, research studying associations between HAP from solid fuel burning and HTN risk has been expanding; we, therefore, undertook a narrative evaluation of systematically identified articles with the aim to summarise recent evidence linking HAP due to biomass fuel and BP or HTN among human participants.

Methods:

Data Sources and Search Strategies: We searched three electronic databases (PubMed, CORE, and Semantic Scholar) for articles published starting from the inception of these databases to March 31, 2022. The search strategy included keywords related to blood pressure and HAP or biomass. In addition, we reviewed the full text of relevant cross-references from each search result.

Article selection: Inclusion and exclusion criteria

Type of study: All randomized controlled trials (RCTs and quasi-RCTs), non-randomized control trials (that is, cohort, case-controlled, and cross-sectional studies), and controlled before-and-after studies were included.

Types of articles: We considered articles published in peer-reviewed journals. Studies or articles that are general and only report HAP, fuel use, and non-indoor or ambient air quality/health-related outcomes were excluded.

After conducting a search on the mentioned databases, all articles were imported into EndNote software (Thomson Reuters 2009) to remove duplicates. After that, a title and abstract screening were conducted, and on the basis of inclusion/exclusion criteria, ineligible articles were excluded. A detailed review of the remaining articles was carried out, and if any of them did not fulfill the inclusion/exclusion criteria, they were further excluded. Figure 1 depicts a chart for this process.

Figure 1: Flow diagram for study selection

Overall, of the total articles obtained through searches in the databases and manual tracking, 28 articles formed part of this review article.

To ensure the unbiased selection and correct identification of articles, two independent investigators conducted an initial screening and examined the full text of each potentially relevant article. If there was any contradiction, it was resolved through discussion among all the authors.

Data extraction: The following information was extracted from all of the included articles: author name, publication year, title of the paper, journal information, geographic location, type of study, study population, sample size and age, sex proportion, fuel type, short-term or long-term effect assessment, type of air pollutant measured, BP measurements, and confounding factors. The information extracted from all of the included articles is detailed in Table 1.

Results

Search results and characteristics of the included studies: As shown in Figure 1, 16,613 articles were identified through a systematically crafted search strategy. After removing duplicate articles and considering the inclusion/exclusion criteria, 92 articles were examined. Among these 92 articles, 65 were excluded after examining the full text because of insufficient data, repeated studies, or research not relevant for inclusion in the current review article. Twenty-eight (28) articles were finally included in this review. Table 1 depicts the summarized data from the 28 included articles.

Pollutants released from solid fuel: Solid fuel combustion produces a large number of health-damaging air pollutants, such as respirable PM, nitrogen oxides, carbon monoxide (CO), formaldehyde, 1,3 butadiene, benzene, polycyclic aromatic hydrocarbons, and many other toxic organic compounds. (15)

Seventeen of the 28 articles have measured the levels of various pollutants emitted by different fuels, including PM, CO, and black carbon (BC).

The majority of the studies (13 out of 28) have measured levels of PM, predominantly PM₁₀ and PM_2.5. The concentrations of PM and time points tested are variable across the studies. The two most commonly used dose metrics are μg/cm² or μg/ml. A summarised version of PM measurement is depicted in Table 2.

Associations between PM and other pollutants exposure and BP: Majority of the research studies included in this review article linking BP or HTN with emissions from solid fuel use focus on PM.

The study done by Young B et al. in rural Honduras showed that traditional stoves produced substantially higher 24-hour mean personal and kitchen PM_2.5 and BC concentrations compared to interventional stoves. The study results provide evidence that one unit increase in kitchen PM_2.5 concentration was associated with 2.5 mmHg higher SBP. However, the associations between kitchen PM_2.5 concentrations and BP were stronger than those for personal PM_2.5, which is contradictory to the general consensus. (16)

These findings are consistent with a randomized intervention study among Guatemalan women, which observed that daily average PM_2.5 exposures were 264 and 102 µg/m³ in the control and intervention groups, respectively. Compared with controls, the intervention group had 3.7 mmHg lower SBP and 3.0 mmHg lower DBP. (24)

Studies by Dutta et al. provide consistent evidence that biomass users who had three times more PM pollution in the kitchen had a higher prevalence of HTN compared to non-biomass users, suggesting a positive association between HAP and increased cardiovascular risk.(30, 31, 33)

Among other components of particulate pollution, several research studies (16,26, 27) have reported higher BP after exposure to BC.

Yet another pollutant which was majorly studied by most researchers was CO. Clark et al. examined the cardiovascular effects of indoor and personal CO concentrations in Nicaragua. They found nonsignificant elevations in SBP due to an increase in 48-hour indoor CO (1.78 mmHg increase in SBP per 24 ppm). Although statistically nonsignificant it is still suggestive of an increase. (25)

Associations between long term exposure to HAP and BP: Multiple studies have shown that long-term exposure (>1 year) to HAP from biomass has positive associations with BP. Table 1 provides a comprehensive summary of the results regarding the long-term impacts of HAP exposures on BP.

Among the numerous articles reported in Table 1, a few of the most notable articles that best exemplify the majority of findings have been chosen for further discussion. In a cross-sectional study conducted by Mohapatra et al. in the Odisha region of India, HTN was found to be associated with the number of cooking years and was also found to be statistically significant in women who regularly cooked with biomass for ≥ 5 years. (15)

Lee et al. showed a significant association between HTN and biomass fuel smoke in China, who had, on average, 19 years of household solid fuel exposure. (20)

A cross-sectional study by Dutta et al. 2011 also indicated that apparently healthy, pre-menopausal, married, non-smoking, tobacco non-chewing women who cook regularly with biomass for the past five years or more showed the prevalence of HTN. Particularly, compared with those cooks having 5–14 years of cooking experience (25.4%), HTN was more prevalent in women cooking for 15 years or more (34.2%) with biomass, although the difference was not found to be significant. (30)

Associations between short term exposure to HAP and BP: Eight articles investigated the short-term effect of HAP on BP values. Young et al. assessed exposure to household air pollution by stove type categories among 147 women in Honduras. After controlling for confounders, women using traditional stoves were nearly twice as likely as women using Justa stoves to have prevalent borderline high or high blood pressure. (16)

Similarly, in a cross-sectional study conducted in three rural communities in Southern Nigeria, the mean SBP among biomass fuel users was 135.3 mmHg compared to 123.8 mmHg among non-biomass fuel users. The mean DBP among biomass fuel users was 83.7 mmHg, compared to 80.1 mmHg among non-biomass fuel users. These differences were statistically significant. (17) Correspondingly, results of another intervention study showed that improved stove intervention was associated with 3.7 mmHg lower SBP and 3.0 mmHg lower DBP compared with controls. (24)

In the study by Pena MB et al., both SBP and DBP were higher by 3.0 and 2.5 mmHg between participants with and without daily biomass fuel use, respectively. Further, the authors found an association between biomass fuel use and both prehypertension and HTN. (22)

Years of Cooking: Findings from a few studies indicate that the duration of exposure to biomass fuels for cooking is an important determinant factor in the deterioration of pulmonary and cardiovascular parameters. Yan et al. measured the solid fuel-related IAP by the years of solid fuel use. The duration of household solid fuel use was classified as zero, fifteen, or more than five years, and the results revealed that users with the longest duration of solid fuel exposure had 1.63% higher SBP, 1.31% higher DBP, and a higher risk of HTN with an odds ratio (OR) of 1.55 than non-users. (22)

Similarly, in another study conducted in China, Lee et al. found that, compared with individuals in the lowest tertile of the duration of solid fuel exposure (<10 years of use), those in the highest tertile of the duration of solid fuel exposure (>25 years of use) had increased odds of HTN. (20) A similar finding also emanated from a cross-sectional study carried out in Bangladesh, which demonstrated that every 1-year increase in cumulative exposure to biomass smoke eventually exacerbated the risk of HTN by 61%. (35)

Age: The rise in BP with age increases the risk of cardiovascular and renal disease, stroke, and type 2 diabetes mellitus. (44) Even a reduction of as little as two mmHg in SBP could lead to 10% lower stroke mortality and 7% lower mortality from ischemic heart disease or other vascular causes in middle age. (45)

According to the study carried out in rural Honduras, the researchers presented evidence that age impacted the associations with continuous SBP, with stronger associations among women who were 40 years of age or older in comparison to women who were younger.(16)

Similarly, the use of biogas was associated with 68% reduced odds of developing HTN in elderly women; however, these effects were not identified in younger women aged 30–50 years. (19)

Lee et al.'s study on the Chinese population also revealed that the association between solid fuel use and risk of HTN was significant among the ≥ 40-year-old group compared to the < 40-year-old group. (20)

Likewise, SBP progressively increased with age in this population, as reported by Baumgartner et al., 2011. Among women > 50 years of age, a 1-log-µg/m³ increase in PM_2.5 exposure was associated with 4.1 mmHg higher SBP and 1.8 mmHg higher DBP. Although PM_2.5 exposure was positively associated with SBP among younger women, the association was not statistically significant.(23)

A considerable positive association was discovered between the age of biomass-using women and SBP and DBP, according to research by Dutta et al. (30, 31). Alexander et al. observed a statistically significant decrease in SBP in women >50 years of age (n=15) 1-year post-intervention, but no significant decrease was seen in women <50 years of age. (39)

In line with the above findings, the study in Albania also showed a significant association between HAP and HTN risk, especially among participants aged 25 to 54 years old than among those aged 15 to 24 years old.(36)

On the other hand, a considerably greater but non-significant pooled effect on SBP was seen among women above the median age of 30 compared to those younger in the multi-country analysis by Arku et al. Although slightly higher, the odds of HTN in older women (≥30 years) did not differ significantly from those in younger (<30 years) women. Similarly, no statistically significant (pooled) interactions between age and solid fuel on BP parameters or odds of HTN were observed.(18)

Effects on either SBP or DBP: In general, an individual's "blood pressure" refers to the pressure measured within large arteries in the systemic circulation. SBP refers to the maximum pressure within the large arteries when the heart muscle contracts to propel blood through the body. DBP describes the lowest pressure within the large arteries during heart muscle relaxation between beating.(45)

While the majority of research linked using biomass fuels to increases in both SBP and DBP, the results of the study by Norris et al. suggest that for rural Indian women using biomass fuels, increases in exposure to BC (about a 100 g/m3 increase) are associated with modest increases only on SBP. (27)

On the contrary, in an intervention study conducted on pregnant Nigerian women, the intervention cookstoves showed the potential to reduce DBP; however, no significant effect was observed on SBP.(40)

Negative Association: Of the 28 study articles, four studies reported a negative association between using biomass for cooking and either SBP, DBP, or HTN.

After adjustment for potential confounders, a cross-section study conducted in rural Pakistan found no association of HTN with the use of biomass for cooking in current users. Also, no associations were apparent in long-term (≥10 years) users and non-users of biomass fuel. Further, this study found no association between the use of biomass fuel and any of the four outcomes studied (hypertension, angina, previous history of heart attack and definite or probable coronary heart disease (CHD) on electrocardiogram (ECG)), even when the comparison was with women who had not used biomass for at least the last ten years.(14)

Similarly, Ofori et al. found a negative association between HAP and HTN. (17) A study performed on pregnant women from central East India also observed a lower risk of maternal HTN associated with the use of wood as cooking fuel.(29) In a large international multi-centre study by Arku et al., chronic exposure to outdoor PM_2.5 was associated with increased BP and HTN but a small inverse association with HAP. The researchers observed a decrease in odds of HTN and a decrease in SBP and DBP among solid fuel users, but these associations varied notably by study country and study centre, with generally positive associations for SBP in China and negative associations in India and in other countries.(18)

Discussion

Burning biomass fuels has remained a primary energy source in many LMICs despite global breakthroughs in the supply of renewable and sustainable energy. (42)

The impact of HAP on BP has been the subject of quite a few meta-analysis and review articles. In the meta-analysis by Liang et al., each increase in PM_2.5 concentration by 10µg/m³ caused a rise in SBP and DBP but long term exposure showed the strongest associations. (46)

One recent meta-analysis, indicated that both short-term and long-term exposure to some air pollutants might increase BP values among children and adolescents.(48)

The literature review by Giorgini et al., revealed that ambient and personal exposure to particulate pollution causes a significant increase in BP. The authors proposed that although consistent data examining both PM₁₀ and PM_2.5 effects exist, future evaluations exploring the impact on BP of personal and mixed air pollution exposure are needed.(13)

These narrative and systematic reviews offered proof that air pollution affects BP, but they were carried out more than three years ago. A thorough assessment of the existing literature was necessary because research on the usage of biomass fuel and its effects on health has been growing in recent years. In order to evaluate the data on the effects of HAP on cardiovascular health through its impact on BP, this review set out to address this question.

Our review reveals that there is a small but growing body of literature on the connection between BP and HAP from solid fuel or biomass. Additionally, there is a lack of consistency in the evidence supporting the claimed link, with some research showing a strong association while others show no association. Further, confounding is an important potential limitation of several studies because sex, age, tobacco use, duration of fuel use, ventilated v. non-ventilated rooms and adoption and socioeconomic status, all these factors are associated with several cardiovascular risk factors, including BP.

To the best of our knowledge, we have presented a thorough analysis of practically all research studies that have investigated an association between at least one component of IAP or HAP and BP, which is a notable strength of our review article. Furthermore, we used three significant databases and a human search of each selected article's bibliography as part of our thorough search approach. Unfortunately, due to a lack of data, we were unable to address all of the confounding factors, including sex, socioeconomic position, sample size, and others, despite our careful and attentive efforts. Additionally, given limitations on the clinical perspective of this review, we have not included studies done in children or adolescent populations. Additionally, the definition of HTN differed from article to article, making the reliability of evidence pointing to a significant connection questionable. Additionally, because the concentrations of air pollution were measured differently in each study, there may have been some degree of exposure misclassification. Finally, since our search was limited to works written in English, it's likely that pertinent research written in other languages went undiscovered.

Conclusion

To conclude, the data imply that even brief exposure to contaminated air, particularly in the enclosed setting of the kitchen, might increase blood pressure, thus increasing the risk of cardiovascular disease. Despite the fact that some studies found that the increase in blood pressure caused by HAP was not statistically significant, such a little increase may nevertheless be enough to precipitate a heart attack or stroke in people who are predisposed to such cardiovascular disorders. Therefore, it is essential to lower HAP from solid fuel, which remains one of the main sources of energy for many families in LMICs. Hence, until everyone has access to cleaner fuels, additional efforts should be made to promote the use of cleaner cooking fuels like LPG in order to limit exposure to solid fuel smoke.

Additionally, the conflicting results, as discussed in this review article, highlight the need for additional research studies that precisely examine the relationship between the usage of solid fuel and preventable cardiovascular risk factors including blood pressure.

Acknowledgement

The authors would like to thank Dr. Laila Garda, Director Research, KEM Hospital Research Centre, Pune, India for her constant guidance and support.

Sources of Funding

This research received no specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

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